Selective attention is a crucial cognitive function that allows one to focus on relevant information in a complex environment. When attention is covertly directed to a location where a stimulus is predicted to appear, processing of stimuli at that location will be enhanced, whereas processing at unattended locations where potential distractors may appear will be suppressed. In adults with typical development, lateralized increases in alpha-band oscillatory activity (8-15 Hz) over parieto-occipital cortices have been well-established as a metric for attentional control using high-density electroencephalography (EEG). In individuals with autism spectrum disorders (ASD), aberrant alpha oscillatory dynamics suggest that brain regions involved in attentional control are atypically activated. Additionally, individuals with ASD have well-documented behavioral impairments in disengaging the focus of attention. These individuals have also shown atypical activations in frontoparietal regions involved in attentional control, and potentially reduced connectivity between key regions in the attentional network. Yet, the neurophysiological deficits in attentional control in ASD have not been clearly established, and it is possible that the neural networks for attentional control are intact, but atypical activations of underlying reward circuitry contribute to attention control deficits in individuals with ASD. The goal of this work is to characterize the neurophysiology of attentional control in ASD and to investigate the role of motivation in regulating these processes. Stimuli that fall within restricted or circumscribed interests (RCI, e.g. trains) are often more motivating to individuals with ASD than social stimuli, and increased motivation has been shown to enhance activation in attention control regions in ASD. It may be that the atypical activation o attentional control circuits to social and non-social cues can be regulated in individuals with ASD through the presentation of motivating RCI stimuli that are contingent on these cues. The guiding model for this work holds that initial neuropathology at birth reduces sensitivity to socia reward, resulting in atypical activation of attention control brain areas, which is propagated by impaired attention to social stimuli and increased attention to stimuli of RCI. In the proposed work, alpha-band EEG indices for anticipatory attentional control will be correlated with standard clinical ASD severity measures for RCI. This will be crucial for understanding the relationship between attentional control deficits and RCI in ASD. A visuospatial cueing paradigm will be used in conjunction with the aforementioned alpha-band EEG metric to examine the integrity of attentional control. Motivational salience of imperative stimuli will be manipulated through presentation of participant-specific RCI stimuli, and anticipatory attentional control will be examined in nonsocial and social domains. The findings of these studies will have relevance for early interventions to regulate atypical neural activations underlying attentional control deficitsin ASD, and improve overall social functioning into adulthood.